A THEORY OF BRAIN CHEMISTRY AND ALCOHOLISM Brain/Mind Bulletin 4/16/84 Why do people abuse alcohol?

Can brain chemistry be altered to break this addiction? People may be driven to drink because of a lack of endorphins in the central nervous system. They may be helped to stop heavy drinking by a recent breakthrough that maintains stable levels of endorphins by inhibiting their breakdown in the brain. Since finding the naturally occurring opioid peptides, scientists have uncovered many links between alcohol and opiates. When people drink heavily, higher levels of these peptides can be found in the blood. At the same time, beta-endorphin has been found to decrease in the cerebrospinal fluid of alcoholics, revealing a depletion in the central nervous system. Naloxone, which inhibits the action of opioids, counteracts alcohol effects in animals and human beings. These and other findings have led psychopharmacologist Kenneth Blum of the University of Texas, San Antonio, to propose a new model to explain why people drink too much. “Lower levels of brain endorphin in alcoholics have several possible causes. They may stem from genetic factors, environmental variables, or some combination of the two.” Blum divides alcoholics into three categories with respect to opioid deficiency: * Type 1 subjects have a desire for alcohol that derives from a genetic deficiency of natural opioids plus stressful environmental conditions, which unmask the deficiency. * Type 2 alcoholics drink because of stressful environmental conditions, which deplete normal stores of natural opiates. * Type 3 subjects are those with a combination of stressful conditions and heavy use of alcohol, both of which lead to a reduction in brain opioid levels. Experimental support for Blum’s hypothesis has grown recently. Unpublished studies in Italy have revealed support for Type 1 alcoholism. According to this theory, people born of alcoholic parents should have lower endorphin levels at birth than do others. So when researchers stimulate production of their brain peptides, smaller amounts would be released. On the other hand, when endorphins are stimulated in non-alcoholics, an increase would be apparent. The Italian investigators tested this theory by using acupuncture to trigger endorphins in people of alcoholic parents. The subjects produced much less compared to people with no family history of alcoholism or to social drinkers. Italian researchers also found evidence for Type 3. They measured endorphin levels in the cerebrospinal fluid of 29 alcoholics. The subjects produced three times less endorphin than other people. At the Max Planck Institute in West Germany, further evidence of Type 3 alcoholism has come to light. In this case, alcohol was seen to act as an opiate, decreasing synthesis of endorphins in the brain.

Compounds known is TIQs are formed as by-products of alcohol when it is broken down in the brain. TIQs bind to neuron receptors normally occupied by opioid peptides. “When the brain sees receptors saturated by TIQs, it stops producing endorphins. It’s a Catch-22,” Blum said. “The more heavy drinkers drink, the more they need to drink.” Evidence for Type 2: Studies in rats have shown that chronic stress, which increases alcohol consumption when the stress is removed, depletes the opiate enkephalin by 50 percent. Strains of mice bred to differ in their preference for alcohol also differ in brain levels of enkephalin. Those with a high preference for alcohol have lower levels of enkephalin than strains that avoid alcohol. So, Blum asked, what intervention would help people maintain normal levels of endorphin, thereby altering heavy drinking patterns? “Now we can alter the metabolism in people who are genetically deficient or under great stress or long-term drinkers. By inhibiting the enzyme involved in endorphin destruction, we can cut off alcoholics’ desire to drink.” Blum has done this successfully in mice bred to drink large quantities of alcohol. “They gained an aversion as strong as those bred to dislike it.” [Kenneth Blum is the author of Abusable drugs, Gardner Press, San Antonio.]

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